DiSilvestro R A
Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907.
J Nutr. 1988 Apr;118(4):474-9. doi: 10.1093/jn/118.4.474.
Serum superoxide dismutase (SOD) activity concentrations, though small compared to tissue levels, could contribute to extracellular superoxide radical detoxification and act as indicators of copper status. The present study identified the response of rat serum SOD activity contents to marginal and deficient copper intakes and to inflammation. Rats fed copper-deficient diet (less than 0.2 mg/kg Cu) for 5 wk displayed serum SOD activity contents that were only about 20% of those found in rats fed copper-supplemented diet (6.0 mg/kg Cu). Activities in rats fed a marginal diet (1.5 mg/kg Cu) were about 55% of those in the adequate rats. Turpentine-induced inflammation lowered serum SOD in rats within each dietary group. However, the change in the marginal group was not statistically significant. Based on chromatographic characterizations and inhibitor studies, rat serum SOD activity seemed to result primarily from a copper protein other than ceruloplasmin, Cu-Zn SOD or the recently discovered tissue extracellular SOD. In conclusion, low copper intake and inflammation may compromise extracellular defenses against superoxide. In addition, serum SOD activities could provide a non-ceruloplasmin-related means of assessing copper status, but nondietary variables can also affect these SOD values.
血清超氧化物歧化酶（SOD）的活性浓度，尽管与组织水平相比含量较少，但可有助于细胞外超氧化物自由基的解毒，并作为铜状态的指标。本研究确定了大鼠血清SOD活性含量对边缘性和缺乏性铜摄入以及炎症的反应。喂食低铜饮食（铜含量低于0.2mg/kg）5周的大鼠，其血清SOD活性含量仅约为喂食补充铜饮食（铜含量6.0mg/kg）大鼠的20%。喂食边缘性饮食（铜含量1.5mg/kg）的大鼠的活性约为正常大鼠的55%。松节油诱导的炎症降低了每个饮食组大鼠的血清SOD水平。然而，边缘性饮食组的变化无统计学意义。基于色谱特征和抑制剂研究，大鼠血清SOD活性似乎主要源于一种不同于铜蓝蛋白、铜锌SOD或最近发现的组织细胞外SOD的铜蛋白。总之，低铜摄入和炎症可能会损害细胞外对超氧化物的防御能力。此外，血清SOD活性可为评估铜状态提供一种与铜蓝蛋白无关的方法，但非饮食变量也会影响这些SOD值。
